Lymph Nodes


The lymph nodes are numerous encapsulated structures occurring in mammalians along the lymphatics. They contain lymphoid cells with a precise microanatomy organised to react to a variety of antigens via humoral and cellular immune responses. Lymph nodes consist of a cortex (B‐cell zone) with primary and secondary follicles, a paracortical region (T‐cell zone), sinuses and medullary cords. High endothelial venules represent a specialised vasculature with specific receptors for immune cells, which facilitate the migration of lymphocytes and dendritic cells. The main function of the lymph node is to generate an efficient immune response to antigens that have penetrated the organism in the areas drained by that node. Follicular dendritic cells present antigen to naïve B cells inside the germinal centres, whereas interdigitating dendritic cells present antigen to naïve T cells in the paracortex. Malignant lymphoma represents the overwhelming majority of primary lymph node neoplasms, including both Hodgkin and non‐Hodgkin lymphomas.

Key Concepts

  • The main function of the lymph node is to generate an immune response to antigens in the drained areas.
  • Most mature lymphocytes constantly recirculate between tissue and peripheral blood every day.
  • High endothelial venules possess specific properties that attract lymphocytes.
  • Germinal centres are created and dominated by a few large B‐cell clones that exhibit intraclonal diversity.
  • Reactive changes and enlargement of the lymph node usually takes an exaggerated form of the normal immune response.
  • Malignant lymphomas represent the overwhelming majority of lymph node neoplasms.

Keywords: cortex; paracortical zone; medulla; sinuses; dendritic cells; high endothelial venules; germinal centres; immune response; lymphoma

Figure 1. Sites of major lymph node groups.
Figure 2. Schematic representation of a lymph node.
Figure 3. (a) Haematoxylin and eosin‐stained section of a lymph node; (b) serial section stained with the B‐cell antigen, cluster designation (CD) 20; (c) serial section stained for the T‐cell antigen CD3 and (d) serial section stained for B‐cell leukaemia/lymphoma (bcl) 2 protein. The cortical areas are the nodules highlighted in the B‐cell stain in (b). The germinal centres are bcl‐2 negative (d). The paracortical region is highlighted in the T‐cell stain in (c). The sinuses are the clear areas unstained in (b), (c) and (d). The medullary cords are the cells stained for B‐cell antigens in (b) adjacent to the innermost (medullary) sinuses.
Figure 4. The secondary follicle is comprised a germinal centre surrounded by a mantle zone layer. The germinal centre is formed when Naïve B cells are activated in the paracortical area, undergo transformation, and clonally expand within hours giving rise to centroblasts. Centroblasts then differentiate into centrocytes, which are positively selected based on the affinity of their B‐cell receptor to process the antigen trapped within the follicular dendritic meshwork. Centrocytes with mutations that decrease their affinity for the antigen are negatively selected and undergo programmed cell death (apoptosis). After an additional heavy chain class switching, the positively selected B cells leave the germinal centre and differentiate into either memory B cells or plasma cells.


Bromley SK and Luster AD (2006) Turning up the heat on HEVs. Nature Immunology 7 (12): 1288–1290.

Butcher EC and Picker LJ (1996) Lymphocyte homing and homeostasis. Science 272 (5258): 60–66.

Girard JP, Moussion C, et al. (2012) HEVs, lymphatics and homeostatic immune cell trafficking in lymph nodes. Nature Reviews Immunology 12 (11): 762–773.

Jaffe ES, Stein H, Campo E, Pileri SA and Swerdlow SH (2008) Introduction and overview of the classification of the lymphoid neoplasms. In: Swerdlow SH, Campo E, Harris NL, et al. (eds) WHO Classification of Tumors of Hematopoietic and Lymphoid Tissues. Lyon: IARC Press.

Kuppers R, Zhao M, et al. (1993) Tracing B cell development in human germinal centres by molecular analysis of single cells picked from histological sections. EMBO Journal 12 (13): 4955–4967.

Liu YJ, Zhang J, et al. (1991) Sites of specific B cell activation in primary and secondary responses to T cell‐dependent and T cell‐independent antigens. European Journal of Immunology 21 (12): 2951–2962.

MacLennan IC (1994) Germinal centers. Annual Review of Immunology 12: 117–139.

Picker LJ and Butcher EC (1992) Physiological and molecular mechanisms of lymphocyte homing. Annual Review of Immunology 10: 561–591.

Przylepa J, Himes C, et al. (1998) Lymphocyte development and selection in germinal centers. Current Topics in Microbiology and Immunology 229: 85–104.

Reis e Sousa C (2006) Dendritic cells in a mature age. Nature Reviews Immunology 6 (6): 476–483.

Sainte‐Marie G (2010) The lymph node revisited: development, morphology, functioning, and role in triggering primary immune responses. Anatomical Record (Hoboken) 293 (2): 320–337.

Warnock RA, Askari S, et al. (1998) Molecular mechanisms of lymphocyte homing to peripheral lymph nodes. Journal of Experimental Medicine 187 (2): 205–216.

Weiss LM (2008a) Benign lymphadenopathies. In: Weiss LM (ed) Lymph Nodes. New York: Cambridge University Press.

Weiss LM (2008b) Normal lymph nodes. In: Weiss LM (ed) Lymph Nodes. New York: Cambridge University Press.

Further Reading

Sousa CR (2006) Dendritic cells in a mature age. Nature Reviews Immunology 6: 476–483.

Swerdlow S, Campo E, Lee Harris N, et al. (eds) (2008) WHO Classification of Tumors of Hematopoietic and Lymphoid Tissues. Lyon: IARC.

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Rezk, Sherif A, and Weiss, Lawrence M(Sep 2015) Lymph Nodes. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000525.pub3]